The monitoring of intracranial pressure is important in the management of head trauma and many neural disorders. Edema associated with many pathologic conditions of the brain may cause an increase in intracranial pressure that may in turn lead to secondary neurological damage. In addition to head trauma, various neurological disorders may also lead to increased intracranial pressure. Examples of such disorders may include intracerebral hematoma, subarachnoid hemorage, hydrocephalic disorders, infections of the central nervous system, and various lesions to name a few.
As a specific example, hydrocephalus is characterized by increased intracranial pressure due to an excess of cerebrospinal fluid, which is often the result of malabsorpition or impediment of clearance in the intraventricular space within the brain or subarachnoid spaces about the brain. Hydrocephalus is often treated by insertion of a diverting catheter into the ventricles of the brain or into the lumbar cistern. Such a catheter or shunt is connected by a regulating valve to a distal catheter which shunts the spinal fluid to another space where it can be reabsorbed. Examples of common diversion sites include the peritoneum of the abdomen via a ventriculoperitoneal shunt or lumboperitoneal shunt or the atrium of the heart via a ventriculoatrial shunt. Although the symptoms of excessive intracranial pressure and associated ventricular enlargement may be relieved by this procedure, it is not uncommon for the shunt apparatus to become obstructed, resulting in shunt failure. An invasive surgery known as shunt revision may be performed to replace or repair the failed shunt. While shunts may become obstructed at a valve or distal tubing level, a great majority of shunt failures are due to proximal obstruction at the tip of the proximal catheter due to gradual growth of scar about the catheter tip or ingrowth of tissue such as choroid plexus into the catheter tip. A wide variety of techniques of positioning of the catheter and various designs have been explored to diminish obstruction, including many modifications of the side inlet holes of the proximal catheter tip. These have met with modest success at best. The routine clinical approach to shunt failure is therefore to replace the obstructed component and to employ higher pressure regulating valves or related valve components to diminish the tendency of overshunting, a condition characterized by the ventricles eventually becoming much smaller than normal and hugging the proximal catheter.
It is not always readily apparent to a clinician that a shunt has failed when a patient having a shunt exhibits early shunt failure symptoms such as headache and nausea. Various techniques have been employed to determine functionality of the shunt. For example, an imaging test of the brain such as CT scan, MRI scan, or ultrasound may show progressive ventricular enlargement compared to previous scans. As another example, shunt failure may be demonstrated by inserting a needle into the shunt valve reservoir and attempting to aspirate. An inability to do so may indicate a failed shunt, however a working shunt in very small or slit-like ventricles may act similarly, thus incorrectly reporting that the shunt has failed. As a further example, flow studies such as radioisotope, ultrasound or MRI may show minimal or no flow. Also, a previously implanted intracranial pressure sensor may provide evidence that the shunt has failed or is failing.
The various shunt functionality tests previously utilized may not be preferred in many circumstances due to a high degree of inaccurate results or due to an unnecessary level of invasiveness. As such, systems and methods for improvement in the accuracy of shunt failure detection due to proximal obstruction, guidance to physicians of the degree of patency of the neural shunt device, and simplified determination of restoration of shunt functionality would impact the management of hydrocephalus and other neural disorders and head trauma.